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Sunlight, Ultraviolet Radiation,
and the Skin

National Institutes of Health
Consensus Development Conference Statement
May 8-10, 1989

This statement is more
than five years old and is provided solely for historical purposes. Due to
the cumulative nature of medical research, new knowledge has inevitably
accumulated in this subject area in the time since the statement was
initially prepared. Thus some of the material is likely to be out of date,
and at worst simply wrong. For reliable, current information on this and
other health topics, we recommend consulting the National Institutes of
Health's MedlinePlus http://www.nlm.nih.gov/medlineplus/.

This statement was originally published as: Sunlight, Ultraviolet Radiation, and the
Skin. NIH Consens Statement 1989 May 8-10;7(8):1-29.

For making bibliographic reference to the
statement in the electronic form displayed here, it is recommended that
the following format be used: Sunlight, Ultraviolet Radiation, and the
Skin. NIH Consens Statement Online 1989 May 8-10 [cited year month
day];7(8):1-29.

Introduction

It is ingrained in humans to love light
and, indeed, since mankind's first wanderings from the caves, worship of
the sun has been a fundamental tenet that many societies hold even to
the present.

The properties of the sun that have
inspired such reverence include its light (visible radiation) and its
warmth (infrared radiation). Additional portions of the solar spectrum
that cannot be perceived directly by the senses (ultraviolet) are
capable of evoking both physiologic and pathologic events in the skin.

Sunlight is the ultimate source of energy
and is vitally important to life as we know it. However, absorption of
incident solar energy by components of the skin can cause a variety of
pathological sequelae.

Until the 20th century, the sun was the
predominant source of human skin exposure to energy within the
photobiologic action spectrum. More recently, artificial devices capable
of mimicking the emission of some or all of the solar spectrum have been
introduced, compounding the opportunities and risks of ultraviolet
radiation (UVR) exposure.

Despite the undeniable importance of
cutaneous exposure to ultraviolet radiation for vitamin D homeostasis,
there is little evidence to indicate that there are additional
beneficial effects of such exposure. Indeed, overwhelming evidence
exists to support the concept that the skin is damaged in many different
ways by its direct exposure to natural or artificial UVR. Some exposure
is virtually unavoidable over a lifetime and is dramatically dissimilar
in different populations depending upon climate, geography, occupation,
and recreational activities. The consequences of this exposure are also
influenced by factors such as the degree of melanin pigmentation. The
effects of UVR can be divided into two general types, acute and chronic.
Acute effects include sunburn, and chronic effects include, among
others, the development of certain forms of skin cancer. In addition,
the skin is a major site of immunologic activity, and UVR is capable of
affecting the immune system via its effects on the skin. The skin is
also susceptible to degenerative changes evoked by chronic UVR. These
changes are a major component of the constellation of physical changes
perceived as skin aging but, which in reality, are due to chronic
photodamage.

It is now possible to measure the effects
of solar radiation on the skin, and epidemiologic studies from around
the world have provided important new knowledge concerning the risks and
benefits of exposure to sunlight and UVR.

Expanding knowledge about the hazards of
exposure to sunlight and UVR has been accompanied by improved approaches
to photoprotection, including the development of more effective
sunscreen formulations. In addition, there is increasing interest in
pharmacologic agents such as the retinoids that may be capable of
inhibiting the development of or possibly even reversing certain chronic
effects of cutaneous sun exposure.

Considerable controversy remains
concerning the specific adverse effects caused by various wavelengths of
UVR, the magnitude of the adverse effects, and potential strategies for
their prevention and/or treatment. A Consensus Development Conference
was undertaken in an effort to define the specific interactions of
sunlight, UVR, and the skin as well as to identify methods for
preventing and/or treating the adverse effects of UVR. Sponsored by the
National Institute of Arthritis and Musculoskeletal and Skin Diseases,
the Office of Medical Applications of Research, the National Cancer
Institute, and the National Institute of Child Health and Human
Development of the National Institutes of Health, the Food and Drug
Administration, and the Environmental Protection Agency, the conference
brought together physicians, scientists, and other health care
professionals, along with representatives of the public on May 8-10,
1989. Following 1 1/2 days of presentations and discussions by the
invited experts and the audience, members of the consensus panel drawn
from the biomedical research community and the public weighed the
scientific evidence in formulating a draft statement in response to
several questions:

What are the sources of ultraviolet
radiation, and is the extent of human exposure changing over time?

In applying the recommendations of this
consensus conference, it is important to recognize that special
circumstances may exist for each patient. These may include unavoidable
exposures to UVR or the inability to use certain of the preventive
strategies. There are clearly some areas in which final recommendations
cannot yet be made due to insufficient data. In these situations,
physicians must use their best clinical judgment in advising patients.

What Are the Sources of Ultraviolet
Radiation, and Is the Extent of Human Exposure Changing Over Time?

There are both natural and artificial
sources of UVR. Although there are many artificial sources of this
energy, sunlight is the only natural source.

The sun emits a wide variety of
electromagnetic radiation, including infrared, visible, ultraviolet A (UVA;
320 to 400 nm), ultraviolet B (UVB; 290 to 320 nm), and ultraviolet C (UVC;
10 to 290 nm). The only UVR wavelengths that reach the Earth's surface
are UVA and UVB. UVA radiation is 1,000-fold less effective than UVB in
producing skin redness. However, its predominance in the solar energy
reaching the Earth's surface (tenfold to one hundredfold more than UVB)
permits UVA to play a far more important role in contributing to the
harmful effects of sun exposure than previously suspected.

Sunlight is the greatest source of human
UVR exposure, affecting virtually everyone. The extent of an
individual's exposure, however, varies widely depending on a
multiplicity of factors such as clothing, occupation, lifestyle, age,
and geographic factors such as altitude and latitude. There is greater
UVR exposure with decreasing latitude. Residing at higher altitude
results in a greater UVR exposure such that for every 1,000 feet above
sea level, there is a compounded 4 percent increase in UVR exposure. UVR
exposure increases with decreased stratospheric ozone. Other factors
that influence exposure to UVR include heat, wind, humidity, pollutants,
cloud cover, snow, season, and time of day.

Solar flares (sunspots) also alter the
amount of UVR reaching the Earth. Solar flares increase ozone
concentration in the stratosphere (above 50 km) thereby reducing the
amount of surface UVB. This 11-year cycle of solar flares causes as much
as a 400-percent variation in UVB at 300 nm reaching the earth. When
solar flares are inactive, there is a decrease in the ozone
concentration, allowing increased UVB to penetrate to the Earth's
surface.

There is also serious concern about
depletion of stratospheric ozone by manmade chlorofluorocarbons (CFC).
These extraordinarily inert chemicals are used in numerous commercial
products, including aerosols and refrigerants. The U.S. Environmental
Protection Agency has been charged with estimating the effects on health
associated with changes in stratospheric ozone levels. In a recent risk
assessment document, the Agency predicted that without controls on CFC
production, there would be a 40 percent depletion of ozone by the year
2075. The Agency further concluded that for every 1 percent decrease in
ozone, there will be a compounded 2 percent increase in the more
damaging shorter UVB wavelengths reaching the Earth's surface. Such an
increase in UVB penetration to the earth is predicted to result in an
additional 1 to 3 percent increase per year in nonmelanoma skin cancer (NMSC).

Recent satellite measurements already
indicate a worldwide decrease in stratospheric ozone over the last
decade. Both satellite- and land-based measurements have revealed a
seasonal hole in the ozone layer over the Antarctic secondary to its
destruction by CFC's. Although increased surface UVB has been measured
in the Antarctic, there has not yet been a measurable change in UVB as a
consequence of CFC's in the stratosphere in the United States.

Over the past several decades, the
average American's exposure to UVB has increased considerably due to
changing lifestyles--more outdoor recreational activities, more emphasis
on tanning, scantier clothing, and a population shift to the sunbelt.

The most common sources of artificial UVR
exposure are various kinds of lamps that emit this form of energy. These
lamps are used primarily for recreational tanning and phototherapy of
skin diseases (e.g., psoriasis and cutaneous T-cell lymphoma (mycosis
fungoides). UVR lamps can emit UVA, UVB, and/or UVC. Those lamps
currently used for recreational tanning emit UVA primarily or
exclusively. Some UVA lamps generate greater than 5 times more UVA per
unit time than solar UVA radiation reaching the Earth's surface at the
Equator. At these doses, "pure UVA" is likely to have adverse
biologic effects. However, UVB remains a potential problem with most of
these sources. Even 1 percent UVB emission from a UVA source can cause a
significant increase in the potential for skin cancer.

The tanning industry is rapidly growing
in the United States. Currently, more than 1 million Americans use
commercial tanning facilities every day. The biggest categories of users
are adolescents and young adults, especially women.

The use of artificial ultraviolet sources
for the phototherapy of dermatologic diseases has increased
substantially in recent years and has exposed a group of people to
markedly increased doses of UVR. Epidemiologic studies of these patients
have shown an unequivocal dose-dependent increase in the incidence of
NMSC, especially squamous cell carcinoma (SCC).

Another potential but as yet unexplored
source of artificial UVR is unshielded fluorescent bulbs used for
illumination. An unresolved issue is the amount of UVA emitted by such
sources and the long-term effects of this exposure. More research is
needed to clarify these problems.

What Are the Effects of Sunlight on the
Skin?

Marked morphologic changes in all parts
of the skin, except perhaps the subcutaneous tissue, are recognized as
consequences of exposure to UVR. These changes underlie the clinically
observed sagging, wrinkling, leathery texture, and blotchy discoloration
of skin typically associated with actinic damage. It is unclear how much
exposure and how much time is required to effect these changes, although
it is evident that clinically normal appearing skin can show pathologic
signs of sun damage upon histologic and ultrastructural examination. It
is known that individuals with fair complexions are more susceptible to
this damage.

In the epidermis UVR-induced changes
include aberrant tissue architecture and alterations in keratinocytes
and melanocytes and functional changes in Langerhans cells. Sun-exposed
epidermis becomes thickened as much as twofold compared to sun-protected
skin and is disorganized, showing evidence of hyperkeratosis,
parakeratosis, and acanthosis. Keratinocytes lose their typical
alignment and progressive flattening, show inclusions in the nucleus,
and accumulate excessive amounts of melanosome complexes above the
nucleus (capping). At the ultrastructural level, clumped keratin
filaments and alterations in electron density of some basal cells are
characteristic. Keratinocytes of the more differentiated epidermal
layers (upper spinous, granular, and cornified) show few, if any,
cytologic changes.

In spite of evidence for morphologic
change, there are no data indicating altered keratinocyte
differentiation as a result of sun exposure. Furthermore, it is not
known how UVR interactions with light-absorbing molecules within the
keratinocytes (e.g., DNA, keratins, lipids) correlate with the changes
in morphology. Two other cells of the epidermis are also affected by UVR.
The melanocyte, with its melanin pigment-containing melanosomes, is the
primary cell involved in photoprotection of the skin. In sun-damaged
epidermis, these cells enlarge, increase in number, and migrate to
higher levels of the epidermis. UVR also affects Langerhans cells in
both animal and human skin by altering their immunologic function. Even
low doses of UVB can reduce their antigen-presenting capability, block
the normal effector pathway, and evoke an inappropriate response by
activating T suppressor networks. It is unclear whether UVR affects
Langerhans cells both directly and indirectly through soluble factors
released by damaged keratinocytes.

The dermal-epidermal junction loses its
rete ridges forming a flattened interface between the epidermis and
dermis. This kind of abutment is more susceptible to shearing forces
than the normal interlocked system of epidermal rete ridges and dermal
papillae. At the ultrastructural level, regions of reduplicated lamina
densa are evident. This change is not unique to photodamage but is
characteristic of trauma to the epidermis by wounding and/or by disease.

UVR causes unique dermal damage such as
alterations in architecture, matrix composition, vascular structure and
function, and cellular activities. The connective tissue immediately
beneath the epidermis (Grenz Zone) contains large bundles of densely
packed, normal-appearing collagen fibrils. Beneath this region, a broad
zone of electron-dense elastotic material is evident. There are no data
that demonstrate how newly synthesized or degraded, previously existing
elastic fibers contribute to this material. Abnormal collagen fibrils
can be admixed with the elastotic substance. Other studies show changes
in the type III:I collagen ratio and an increase in glycosaminoglycans.
Fibroblasts appear to be metabolically active. It is not clear whether
this is a transient response to the UVR or whether there is a change in
cell phenotype that can be retained in vitro. The mechanisms for
the altered connective tissue responses are not understood. Dermal
vessels become dilated, leaky, and accumulate excessive basement
membrane-like material. Inflammatory cells collect around the vessels;
mast cells are increased and may show evidence of degranulation and
apparent physical associations with fibroblasts. Although the nature of
this relationship is unknown, it is a common observation in other
disorders in which fibrosis occurs.

Sunburn is UVR-induced erythema of the
skin caused by vasodilatation of dermal vessels. This may be mediated
through cyclo-oxygenase and lipoxygenase products of arachidonic acid.
Generation of the prostaglandins associated with UVB erythema produced
within the first 6 to 12 hours can be blocked by topical nonsteroidal
anti-inflammatory agents such as indomethacin. These anti-inflammatory
agents, however, cannot inhibit the delayed, post 24-hour erythema that
is modulated by lipoxygenase products. The time-dependent release of
varying mediators during the UV-induced inflammatory process underscores
the need for further exploration into selective inhibitors of both the
cyclo-oxygenase and lipoxygenase pathways in the prevention and
treatment of sunburn erythema.

Also associated with UVR irradiation of
human skin is the appearance of dyskeratotic keratinocytes, known as
sunburn cells, in the superficial layers of the epidermis. The
mechanisms of the development of these cells are still unclear and
warrant further exploration.

Tanning is the term applied to the
increase in melanin pigmentation following UVR exposure. It is mediated
by a combination of immediate pigment darkening (IPD) and delayed
pigment darkening (DPD). IPD is caused by UVA and is due to
photo-oxidation of preformed melanin. It is not protective against UVB
erythema. DPD occurs about 72 hours after UVR exposure and does not
afford much protection against UVB erythema and pyrimidine dimer
formation. It is accompanied by an increase in the number of DOPA-positive
melanocytes, an increase in the number and melanization of melanosomes,
and an increase in dendricity of melanocytes. The degree of protection
afforded by melanin is unclear. Individuals with dark complexions are
still susceptible to UVR-induced photodamage. UVR also increases the
transfer of melanosomes from melanocytes to keratinocytes. Following UVR
melanosomes diffusely distributed within keratinocytes collect above the
nucleus, forming a "cap" over it. DPD occurs with either UVB
or UVA. DPD induced by UVB is more protective against UVB erythema than
is DPD induced by UVA. Both UVB- and UVA-induced DPD protect equally
well against UVB dimer formation.

In addition to certain genetic and
metabolic disorders that are precipitated by UVR, there are many
photosensitive diseases of unknown cause. These include lupus
erythematosus and polymorphous light eruption, which are elicited by
certain wavelengths of the UVR spectrum. Photosensitivity disorders may
also occur due to the interaction of UVR with many commonly used drugs,
as well as chemicals used in industry and consumer products.

UVR modifies local and systemic immune
responses, functionally alters Langerhans cells, and activates the T
cell suppressor pathway. Soluble factors released from UV-irradiated
epidermal cells also may be responsible for this altered immune
response. In certain experimental systems, UVR-induced tumors
transplanted into genetically identical animals are normally rejected.
If these host animals are UV-irradiated before transplantation, the
tumor will be accepted. These conclusions are based on animal studies.
The role of UVR in the immunobiology of human skin cancer and,
particularly, in susceptibility against certain cutaneous infectious
diseases is unclear. More studies on the effect of UVR on human
neoplastic and infectious disease are warranted.

There is extensive epidemiological
evidence supporting the direct role sunlight plays in human skin cancer.
Basal cell carcinomas (BCC), the most common skin cancers in Caucasians,
are found primarily on sun-exposed areas such as the head and neck where
a dose-response relationship exists. Furthermore, patients with skin
cancer generally have decreased melanin pigmentation and associated
photo-protection; people with light complexion and who sunburn easily
have a higher incidence of tumors. There is even stronger evidence for
the role of sunlight in causing SCC's. Although both BCC's and SCC's are
more prevalent in geographic areas of high sun exposure, there is a much
greater increase in SCC with decreasing latitude and increasing sun
exposure. A reasonable correlation exists between sunlight exposure and
melanoma, but the relationship is not as clear as with NMSC. It should
be emphasized that the incidence of NMSC and melanomas has been steadily
increasing. Unlike NMSC, melanomas occur most frequently on the upper
back in males and lower extremities in females. Melanoma incidence does
not follow a pattern of increased risk with cumulative UVR exposure
whereas the incidence of NMSC does.

Extensive data also exist concerning UVR-induced
skin cancer in experimental animals. In mice and guinea pigs, UVR
induces mainly SCC whereas in rats both SCC and BCC are produced by
repeated doses of UVR. In general, UVR induces SCC's in mice somewhat
more effectively in young animals than in older ones. The cancer
response is preceded by photodamage to the epidermal DNA, inflammation,
epidermal hyperplasia, and dysplasia. Although there are several animal
models in which chemical carcinogens can induce melanomas, the induction
of melanomas by UVR has been very difficult if not impossible. Recent
studies suggest that the opossum may be a reasonable model for UVR-induced
melanomas.

Experiments in animals indicate that UVB
is much more effective than UVA in causing NMSC. Nevertheless, UVA can
induce DNA damage, erythema, and SCC in both pigmented and albino mice
and in guinea pigs. Recent evidence suggests that the longer UVA
wavelengths (UVA I:340 to 400 nm) of the UVA spectrum are less damaging
than the shorter UVA wavelengths (UVA II:320 to 340 nm), but further
research is needed to confirm this distinction.

The exposure of skin to UVB is essential
for the endogenous production of vitamin D3. In areas of the
world where there are inadequate levels of nutritionally available
vitamin D, UVB is the only source. The relationship of sunshine to
vitamin D3 and the normal growth and development of the
skeleton is well known. Exposure of skin to UVR in the region of 290 to
315 nm is essential for the formation of vitamin D3 in the
epidermis.

There is evidence that vitamin D3
synthesis is inhibited by the use of sunscreens. In the United States,
this does not represent a health hazard for the pediatric population
that receives adequate vitamin D supplementation in milk. In other
countries this may not be the case. Deficiencies in elderly populations
may exist.

What Factors Influence Susceptibility to
Ultraviolet Radiation?

Susceptibility to damage by UVR may be
influenced by genetic and acquired disorders, genetic traits,
age-related factors, and the use of some medications.

Genetic abnormalities can increase the
susceptibility to UVR damage. These include disorders manifested in
utero that may be lifelong or that may appear shortly after birth.
Among them are disorders of keratinization and pigmentation. Several
inherited disorders in which there is marked susceptibility to UVR in
early childhood include xeroderma pigmentosum, Bloom's syndrome,
Rothmund-Thomson syndrome, the porphyrias, phenylketonuria, dysplastic
nevus syndrome, and the basal cell nevus syndrome.

Significant factors that influence
susceptibility to UVR damage include race, ethnicity, eye and hair
color, and the tendency toward formation of freckles and nevi. One
approach to categorizing humans in terms of susceptibility to UVR is
typing according to history of sunburning and tanning. Six skin types
have been defined. Type I individuals always burn and never tan; type VI
individuals always tan and never burn. The age of an individual may be
correlated with factors that influence the susceptibility to UVR. These
may include age-related structural differences in the skin, behavioral
differences (e.g., adolescent risk taking) and, hypothetically,
age-related immunological differences.

Numerous systemic medications may augment
UVR susceptibility. Increased UVR damage may occur with the use of oral
antibiotics, antihypertensives, psoralens, immunosuppressive agents,
nonsteroidal anti-inflammatory drugs, and numerous other agents. In
addition, a number of topical medications and industrial chemicals may
increase the susceptibility to damage by sunlight. These include topical
psoralens, tretinoin, and other photosensitizing and depigmenting
agents.

Can Ultraviolet-Induced Changes Be
Prevented? If So, How?

Skin cancers in which UVR exposure plays
an important role are the most common form of cancer. In 1978, there
were more than 500,000 new cases of skin cancer. This is probably a
substantial underestimate for 1989, because the number of office visits
for NMSC has increased more than 50 percent in the past decade while the
overall increase in office visits has only been 11 percent. Therefore,
it is imperative to consider ways to minimize the deleterious effects of
UVR.

What measures can be taken to diminish
the risk of UVR exposure? There is considerable information that can
serve as a basis for developing a policy of "low-risk"
behavior.

First, susceptibility to UVR damage
can be reduced through use of proper clothing made of tightly
woven fabrics with long sleeves, long pants, wide-brimmed hats, etc.

Second, a significant reduction in
certain types of UVR damage can be achieved through the proper use
of physical and chemical sunscreening products. Maximum
photoprotection is afforded by chemical sunscreens with SPF ratings
of 15 or higher. Although most sunscreens on the market today are
appropriate for UVB protection, combination sunscreens that are
effective against UVB and at least part of the UVA spectrum are
preferable. Waterproof sunscreens should be selected by swimmers and
those who perspire sufficiently to wash off nonwaterproof products.
Daily use is recommended during appropriate times throughout the
year. Sunscreens should be applied before exposure, with frequent
reapplications thereafter.

Third, one must strive to enhance
behavior that limits sun exposure. Data exist to suggest that
50 percent of an individual's total lifetime UVR exposure occurs by
18 years of age. Therefore, parental education with subsequent
direction of the behavior of children is important during childhood.
Modified schedules for outdoor activities at school, camp, daycare
centers, or the beach should be considered whenever possible so as
to minimize UVR exposure. Time of day and time of year have a major
impact on the extent of UVR exposure. For example, on a sunny day in
June between 10:00 a.m. and 3:00 p.m., fully 60 percent of the daily
UVB radiation reaching the Earth's surface arrives during this
period. If exposure during this time could be minimized, a
significant reduction in the number of NMSC's would almost certainly
occur. Adults and children should limit their exposure during this
peak period of UVR.

Fourth, one must be aware of photosensitizing
medications and chemicals because it is known that these can
exacerbate the effects of UVR exposure.

Fifth, the adverse effects of
intentional UVR exposure must be considered. All evidence
indicates that UVR-induced suntanning, whether from natural or
artificial sources, is harmful to the skin.

There is a critical need to educate the
public about all of these factors, consideration of which will show that
the low-risk strategies described above are compatible with normal,
active lives.

Sunlight-induced adverse skin alterations
include NMSC, melanoma, actinic keratoses, as well as textural and
pigmentary changes characteristic of chronic photodamage. All of these
cancers are treated by standard surgical techniques. Precancerous
lesions such as actinic keratoses are treated by topical chemotherapy
(e.g., by the use of 5-fluorouracil) and physical methods of superficial
skin destruction (e.g., cryosurgery). Various therapies to improve the
features of chronic photodamage (scaliness, coarse and fine wrinkling,
telangiectasis, and irregular pigmentation) including chemical peels,
the topical use of 5-fluorouracil, alpha-hydroxy acids, and all-transretinoic
acid have been tried. Although the beneficial cosmetic effects of some
of these treatments have received wide publicity, there are insufficient
data demonstrating sustained improvement, reversibility of tissue
pathology, or the preservation of normal skin function by those agents.
There is no information regarding long-term positive, negative, or toxic
effects of these agents. Conflicting data exist demonstrating both
prevention and potentiation effects of topical retinoids in the
development of UVR-induced skin tumors in animals. There are indications
that systemic use of beta-carotene and certain retinoids may be
beneficial in prevention of sun damage in people with certain disorders.
Long-term, large-scale studies of normal individuals in the general
population are in progress.

What Are the Directions for Future
Research?

The following recommendations for future
research are not listed according to any particular priority.

There is a need for updated
epidemiologic data concerning NMSC in the United States. Evidence
exists to suggest that the incidence of NMSC is increasing, but no
new data have been obtained since 1978.

There is a need for more research to
define the action spectra of sunlight and UVR in the pathogenesis of
cutaneous melanoma and to develop better animal models for the study
of this disease.

Studies are needed to define more
precisely the phenomenon known as "photoaging" of the skin
and to compare this with chronologic aging insofar as
pathophysiological mechanisms are concerned.

Studies are needed to better define
the immunological effect of UVR exposure and its potential role in
the development of skin cancer and cutaneous infections.

In particular, the biological effects
of UVA radiation require further study, particularly with the
increased use of UVB sunscreens and UVA tanning equipment, both of
which result in increased UVA exposure.

The importance of UVB radiation in
vitamin D homeostasis requires additional study; alternatives to sun
exposure should be considered as sources of vitamin D.

New approaches for behavior
modification and education are needed to reduce skin exposure to UVR
during childhood and adolescence because it is estimated that as
much as 50 percent of an individual's lifetime sun exposure occurs
by 18 years of age.

More effective sunscreens and nontoxic
anticarcinogenic agents should be developed as approaches to
diminishing the risk of UVR exposure.

The risk/benefit ratio of widespread,
long-term sunscreen use should be monitored.

There is a need for more research in
age-related optical properties of skin and acute and chronic
cutaneous responses to UVR.

There is a need for epidemiologic
study of individuals who use sunscreens that block UVB radiation.

Data are needed that quantitatively
assess UVR exposure in normal populations at all ages and under
various conditions.

Conclusions and Recommendations

Human exposure to UVR from natural
sunlight and artificial sources is increasing substantially.

UVR in sunlight is critical for
vitamin D synthesis in the skin. However, it produces a variety of
pathologic effects, including sunburn, pigmentary change,
immunologic alterations, and neoplasia. A constellation of
structural alterations of the epidermis, the dermal-epidermal
junction, and the dermis is uniquely characteristic of photodamage.

UVR-induced changes can be minimized
or prevented by the use of proper clothing, appropriate application
of physical and/or chemical sunscreens, behavior modification, and
awareness of photosensitizing medications.

Sunlight-induced adverse skin
alterations can be treated by standard surgical techniques and
superficial destructive modalities. There is insufficient evidence
concerning the reversibility of adverse effects by topical and
systemic agents.

There should be better education of
the public with regard to the hazards of tanning parlors, and there
should be greater regulation of tanning facilities to protect the
public against inadvertent injury by UVR.

Consensus Development Panel

David R. Bickers, M.D.
Professor and Chairman
Department of Dermatology
Director
Skin Diseases Research Center
Case Western Reserve University and University Hospitals
Cleveland, Ohio

Donald E. DeWitt, M.D.
Associate Professor
FPC-Department of Family Medicine
East Carolina University School of Medicine
Greenville, North Carolina

Robert S. Gilgor, M.D.
Clinical Professor of Dermatology
University of North Carolina School of Medicine
Dermatologist, Private Practice
Chapel Hill, North Carolina

Robert W. Makuch, Ph.D.
Associate Professor of Biostatistics
Director of Biostatistics Consulting Unit
Director of Clinical Research Office
Department of Epidemiology and Public Health
Yale University School of Medicine
New Haven, Connecticut

Michael Martin, M.D., M.P.H., M.B.A.
Assistant Clinical Professor
Department of Epidemiology and International Health
University of California at San Francisco
San Francisco, California

Lawrence A. Schachner, M.D.
Professor of Dermatology and Pediatrics
Director
Division of Pediatric Dermatology
University of Miami School of Medicine
Miami, Florida

Leonard C. Harber, M.D.
"Real and Potential Adverse Effects of High-Intensity UVA Light
Sources Used for Cosmetic Purposes (Tanning Parlors)"
Chairman
Department of Dermatology
Columbia University College of Physicians and
Surgeons
New York, New York

Michael F. Holick, M.D.
"Role of Sunlight for Producing Vitamin D3 in the
Skin"
Department of Medicine
Boston University School of Medicine
Boston, Massachusetts

Robert S. Stern, M.D.
"Modulation of Effects of Ultraviolet Radiation Based on Presence
of Photosensitivity Disease or Because of Phototherapy"
Department of Dermatology
Massachusetts General Hospital
Boston, Massachusetts

Planning Committee

David R. Bickers, M.D.
Panel and Conference Chairperson
Professor and Chairman
Department of Dermatology
Director
Skin Diseases Research Center
Case Western Reserve University and University Hospitals
Cleveland, Ohio

Linda W. Blankenbaker
Program Analyst
Office of Medical Applications of Research
National Institutes of Health
Bethesda, Maryland

Patricia Blessing
Information Specialist
National Institute of Arthritis and Musculoskeletal and Skin Diseases
National Institutes of Health
Bethesda, Maryland

Delbert Dayton, M.D.
Chief
Genetics and Teratology Branch
National Institute of Child Health and Human Development
National Institutes of Health
Bethesda, Maryland

John Epstein, M.D.
Clinical Professor of Dermatology
University of San Francisco
San Francisco, California